A Review of the Problem of Lead Poisoning in Waterfowl

Diagnosis of Lead Poisoning

Symptoms

The clinical symptoms of lead poisoning in waterfowl have often been described,
and a thorough summary is found in Forbes and Sanderson (1978: 255-256). Some
of the earlier studies (Grinnell 1901; Phillips and Lincoln 1930) describe lead-poisoned
ducks, geese, and swans (Cygnus spp.) as unable to fly, as sick often with
little loss of body weight, as having a rattling in the throat, as so weak as
to be easily captured, and as occasionally dribbling a yellowish fluid from the
bill - which is held open much of the time. Remains of lead pellets are often
found in the gizzards of lead-poisoned waterfowl. The inner lining of the gizzard
is dark, soft, decayed, easily eroded, inflamed, corroded, and incomplete. Often
the bird cannot fly (and later cannot walk) because of progressive paralysis of
the muscles of the wings and legs. On land the tips of the primaries drag the
ground and on water the wings float loosely on the surface. The proventriculus
is often distended, thin and watery green-stained feces are common, and the voice
of geese is often changed.

Like some of the earlier studies, several subsequent studies (Quortrup and
Shillinger 1941; Jordan and Bellrose 1950; Rosen and Bankowski 1960) did not
stress the loss of body weight that is characteristic of chronic lead poisoning
in waterfowl. Bellrose (1964) reported that waterfowl starving because of lead
poisoning weighed about 50% of normal, but Trainer and Hunt (1965) found no
correlation between the body weights of swans with more than 100 lead pellets
in their gizzards and swans with 10 or fewer pellets.

Generally, captive waterfowl that die of chronic lead poisoning lose
from 40 to 60% of their body weight before death; they also lose a greater percentage
of body weight during mild weather than during cold weather. On the other hand,
captive waterfowl that die of acute lead poisoning may lose relatively
little weight before death. W.L. Anderson (1975) also found a direct correlation
between body weight and number of lead pellets in gizzards of wild ducks that
had died of acute lead poisoning. Sanderson and Irwin (1976: Table 16) reported
that 8 of 20 male game-farm mallards on a diet of corn and dosed with five No.
4 lead pellets on 1 July died of acute lead poisoning an average of 7.6 days
later after losing 20.5 percent of their body weight. The 12 remaining ducks
died of chronic lead poisoning an average of 20.7 days after dosing and had
lost 47.6 percent of their body weight. Waterfowl in the wild, we assume, would
follow patterns similar to those of captive waterfowl.

Reports vary concerning the effects of lead poisoning on the appetites of
waterfowl, and the topic merits further investigation. Early workers (Phillips
and Lincoln 1930; Shillinger and Cottam 1937; Quortrup and Shillinger 1941;
Adler 1942) indicated that lead-poisoned waterfowl showed no decrease and sometimes
showed an increase in appetite. Beer and Stanley (1965) found that many birds
that had died of lead poisoning had eaten shortly before death. Other investigators,
however, have reported that lead poisoning causes a loss of appetite and that
a decreased intake of food is one of the earliest external symptoms in lead-poisoned
birds. Jordan and Bellrose (1951) found that captive mallards not dosed with
lead but fed only the amount of food eaten by paired ducks dosed with lead showed
weight loss and other symptoms that were similar to those shown by the lead-poisoned
ducks. Irby et al. (1967) reported that ducks decreased their consumption of
corn for 1-3 weeks after dosing with lead. During the second half of the experiment
(the second month), however, the surviving dosed ducks ate as much or more corn
than did their controls. Irwin et al. (1974) found that adult game-farm mallards
dosed with lead and fed corn had reduced appetites but that dosed ducks fed
an "adequate" diet (among other components, the adequate diet contained 19.2
percent protein compared with 8.8 percent protein in corn) showed no loss of
appetite. Sanderson and Irwin (1976:63) did not measure food consumption in
their studies; however, they noted decreased consumption of corn in ducks dosed
with lead. In some instances, they found that shortly before ducks died of lead
poisoning, their appetite for corn returned.

Quortrup and Shillinger (1941) reported that distention of the proventriculus
and esophagus occurs because food cannot pass the gizzard. In one group of 70
captive mallards, Sanderson and Irwin (1976:63, Table 62) found that only 1
bird of 17 that died of lead poisoning from 4 to 8 days after dosing with lead
had food in the digestive tract; none of the 17 showed impaction. In the same
group of 70 ducks, among those that died from 9 through 39 days after dosing,
7 (10.0 percent) had corn in the esophagus and 2 (2.9 percent) had the esophagus
impacted with corn; 26 (37.1 percent) had corn in the proventriculus and 7 (10.0
percent) had the proventriculus impacted with corn; 53 (75.7 percent) had corn
present in the gizzard and 1 (1.4 percent) had the gizzard impacted with corn.

Diagnostic Techniques and Their Results

In spite of several clinical symptoms for lead poisoning in waterfowl, researchers
cannot always be certain that an individual bird has died of or is suffering
from lead poisoning. Many symptoms are seen only at necropsy. Recently, however,
several diagnostic techniques, some of which can be used with live birds, have
been described.

Bone analysis
Although no individual relationship has been found between the amount of lead
shot in a gizzard and lead residues in wing bones, a significant correlation
between the two occurs on a population basis (White and Stendell 1977:472).
The amount of lead in gizzards of mallards and pintails was closely related
to the amount of lead in their wing bones as reported by the U.S. Fish and Wildlife
Service (1978) and by W.L. Anderson (1975) for lesser scaups at Rice Lake, Illinois.
Lead appears almost immediately in the wing bones after lead shot are ingested
by birds. Thus, ducks that have expelled eroded pellets from their digestive
tracts show an absence of gizzard lead but retain lead residue in their wing
bones.

Wing bones (radii-ulnae) collected at random from 4,190 ducks during the National
Waterfowl Wing Survey in 1972 and 1973 were analyzed for lead by the WARF Institute
of Madison, Wisconsin, for the U.S. Fish and Wildlife Service (Stendell et al.
1979). Bones of adults contained concentrations of lead about twice as high
as concentrations found in juveniles. Lead levels were highest in the Atlantic
Flyway, at moderate levels in the Mississippi and Pacific flyways, and lowest
in the Central Flyway.

A bimodal distribution of lead was found in most of the immature mallards
with wing bones containing lead; the higher levels were believed to be the result
of shot ingestion. About one-third of the wings analyzed from immature mallards
had high levels of lead: 37.5 percent in the Mississippi Flyway, 36.6 percent
in the Pacific Flyway, and 21.2 percent in the Central Flyway (Stendell et al.
1979). Moreover, these birds were only a few months old and had been exposed
to heavily hunted areas for 4 months at most. Elevated lead levels ranged from
8.5 to 82.3 ppm, with a mean of 24.4 ± 17.3, and were found in samples
from various states.

When penned year-old mallards were dosed with one No. 4 lead pellet, concentrations
of lead in the wing bones of laying hens proved to be more than 4 times higher
than levels found in the wing bones of nonlaying hens (Finley and Dieter 1978).
Apparently the mobilization of calcium for egg laying increased the absorption
of lead from the blood stream. In a similar but earlier experiment, Finley et
al. (1976) found high levels of lead deposition in skeletons of laying hens;
these levels may have resulted from calcium mobilization from bones during eggshell
formation. According to Stendell et al. (1979), the lead content of bones is
similar in males and females outside of the breeding season.

Blood analysis
Blood samples have been used to determine the extent of lead toxicosis in waterfowl
populations. The level of blood lead considered toxic but sublethal is 0.5 ppm,
and the U.S. Fish and Wildlife Service recently established ≥0.2 ppm
as a level above background levels. As demonstrated by Dieter (1979) in an examination
of blood from 400 canvasbacks from Chesapeake Bay and the Upper Mississippi
River, 1974-1978, symptoms of lead toxicity began to appear at 0.2 ppm. At levels
of 0.5 ppm and higher (average 0.58 ppm), 12 percent of the canvasbacks showed
significant depression of delta-aminolevulinic acid dehydratase (ALAD) enzyme
activity. A reduction of ALAD enzyme activity in the brain causes cerebellar
damage (Dieter and Finley 1979). Biochemical lesions in the brain precede such
external symptoms of lead poisoning as wing droop and vent staining.

The level of protoporphyrin (PP) in the blood has also been used to determine
levels of lead toxicosis in waterfowl. Roscoe et al. (1979) found that PP levels
exceeding 40 ppm indicate lead poisoning; at 500 ppm an impairment of motor
functions occurs. Motor functions of the nervous system correlate and control
muscular activity. PP is important because it is a precursor to hemoglobin and
because PP increases in the blood of lead-poisoned waterfowl, thereby indirectly
indicating the amount of lead in the blood.

Anderson and Havera (1985) evaluated three methods of determining lead poisoning
in Illinois waterfowl: (1) lead in blood, (2) PP in blood, and (3) ingested
lead pellets in gizzards. They concluded that the lead level in blood was the
most sensitive indicator of toxicosis, the PP level was less so, and the presence
of ingested lead pellets was least likely to indicate the degree of exposure
to lead. They found that 8.1 percent of the blood samples from 1,135 mallard
in 4 areas in Illinois had lead levels of ≥0.5 ppm. Of blood samples
from 864 Canada geese at 3 locations, 6.5 percent had ≥0.5 ppm lead
levels. Fifteen (5.7 percent) of the blood samples from 264 canvasbacks collected
in March from the Keokuk Pool on the Mississippi River had ≥0.5 ppm
lead.

Analysis of the liver and other organs
A number of studies have used the analysis of heavy metals in the livers of
waterfowl as a measure of exposure to lead. Adrian and Stevens (1979) emphasized
the importance of using liver samples that are oven-dried to a constant weight;
wet weights were found to produce sizeable errors.

In dead and moribund lesser scaup collected at Rice Lake, Illinois, W.L. Anderson
(1975:267) found means of 47 and 43 ppm (wet weight) lead in livers of males
and females, respectively; 62 and 77 ppm (wet weight) in kidneys; and 34 and
55 ppm (wet weight) in wing bones. He reported a high correlation between lead
in the livers and lead in the wing bones of female scaup.

An analysis of Canada geese, victims of lead poisoning in eastern Colorado,
disclosed an average lead level of 102 ppm in livers, 125 ppm in kidneys, and
41 ppm (dry weight) in wing bones (Szymczak and Adrian 1978: 301). A high correlation
between the lead concentration in the liver and the concentration in the kidneys
of the same specimens was reported.

Scanlon et al. (1980) examined waterfowl taken by Maryland hunters and compared
the number of birds with ≥10 ppm lead in their livers (dry weight)
and the presence or absence of ingested shot. They found that 28.8 percent of
the waterfowl with shot in the gizzards had ≥10 ppm lead in their
livers but that 16.2 percent of the birds without lead in their gizzards had
equally high levels of lead in their livers. Of 613 specimens representing 14
species, 18.8 percent had liver lead of ≥10 ppm.

At Catahoula Lake and Lacassine National Wildlife Refuge, Louisiana, 1,110
dead and incapacitated waterfowl were collected for liver analysis and shot
ingestion (Shealy et al. 1982). A level of 6.0 ppm wet weight or 20.0 ppm dry
weight was used to indicate lead toxicosis. Of the entire sample, 74.8 percent
had liver lead at those levels or higher. Lead toxicosis, as determined by levels
of lead in livers, was distributed among species as follows: pintails, 82.2
percent; mallards, 80.0 percent; snow geese, 77.2 percent; whitefronted geese,
68.6 percent; and canvasbacks, 52.4 percent. The ingestion of lead shot among
species was comparable: 75.0 percent of the pintails, 68.3 percent of the mallards,
76.9 percent of the snow geese, 71.0 percent of the white-fronted geese, and
60.9 percent of the canvasbacks contained ingested lead pellets. The average
number of pellets ingested for pintails was 3.9; for mallards, 4.2; for snow
geese, 2.0; and for white-fronted geese, 5.4 (Zwank et al. 1985).

The effect of lead poisoning on the size of certain internal organs may differ
according to species and the stage of toxicosis and its nature - acute or chronic.
Several investigators (Coburn et al. 1951; Jordan and Bellrose 1951; Locke and
Bagley 1967; and Bates et al. 1968) found smaller-than-average livers, kidneys,
hearts, and spleens in waterfowl suffering from lead poisoning. In contrast,
Chupp and Dalke (1964) reported large livers in swans that died from lead poisoning
from mine wastes in Idaho. Adler (1944) also reported enlarged kidneys, spleens,
and livers in 4 wild lead-poisoned Canada geese in Wisconsin.

Sanderson and Irwin (1976) agreed that lead toxicosis results in a reduction
of liver size. They also pointed out that the effect of lead on the liver of
ducks is confounded "by the effects of seasons and their differing influences
on the total rate of food consumption and on the relative rates of food consumption
by the sexes, the average postdosing survival time, diet, and the lead-induced
results of anorexia" (p. 30A). They also found that "the mean weights of livers
of most dosed ducks were heavier than livers of undosed controls." They had
no explanation for the heavy livers in dosed ducks, but they also found (p.
62) that the mean weights of livers, spleens, and testes of lead-dosed ducks
that survived to the end of the experiment were significantly heavier than the
mean weights of these organs for all lead-dosed ducks that died during the experiment.

Other techniques
Locke et al. (1966) found that acid-fast inclusion bodies in the proximal convoluted
tubules of the kidneys can be used as presumptive evidence of lead poisoning
in mallards, but this technique does not work for Canada geese (Locke et al.
1967).

Barrett and Karstad (1971) reported that erythrocytes from lead-poisoned Canada
geese and mallards subjected to blue-ultraviolet light showed red fluorescence.
This quick and simple technique can be used on live birds and is as reliable
as some of the more conventional techniques.

One of the common characteristics of lead-poisoned waterfowl is severe anemia
(Beer and Stanley 1965). The main sources of this anemia are probably the production
of defective red cells and the impaired release of red cells (Bates et al. 1968).
Hemosiderosis commonly occurs in kidneys, livers, and spleens of lead-poisoned
waterfowl.

Calcium versenate (Ca EDTA) injected intraveously is diagnostic for heavy
metals. If a live, lead-poisoned bird is injected with Ca EDTA, the symptoms
do not reappear for about 48 hours (Rosen and Bankowski 1960). Several intraperitoneal
injections of Ca EDTA in a solution of 6.6 percent cause lead-poisoned ducks
to regain their appetites and to recover (Wobeser 1969).

For a discussion of several other methods of diagnosing lead poisoning in
waterfowl, see Forbes and Sanderson (1978:256-260).